Review

Journal of Molecular Medicine

, Volume 84, Issue 6, pp 469-477

First online:

Fibrin(ogen) and its fragments in the pathophysiology and treatment of myocardial infarction

  • Kai ZacharowskiAffiliated withMolecular Cardioprotection and Inflammation Group, Department of Anesthesia, University Hospital of Düsseldorf Email author 
  • , Paula ZacharowskiAffiliated withMolecular Cardioprotection and Inflammation Group, Department of Anesthesia, University Hospital of Düsseldorf
  • , Sonja ReingruberAffiliated withFibrex Medical Research and Development
  • , Peter PetzelbauerAffiliated withDepartment of General Dermatology, Medical University

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Abstract

The occlusion of a coronary artery leads to ischemia of the myocardium, while permanent occlusion results in cell death and myocardial dysfunction. Early restoration of blood flow is the only means to reduce or prevent myocardial necrosis, but—paradoxically—reperfusion itself contributes to injury of the heart. In animal models, this phenomenon is well described, and there are many different unrelated approaches to reduce reperfusion injury. In humans, however, pharmacological interventions have so far failed to reduce myocardial reperfusion injury. We summarize the pathogenesis of reperfusion injury, detailing the role of fibrin(ogen) and its derivatives. Moreover, we introduce a new concept for fibrin derivatives as potential targets for reperfusion therapy.

Keywords

15–42 Fibrin fragments Endothelial cell VE-cadherin Leukocyte transmigration Myocardial infarction and reperfusion injury